Pediatric Annals

Special Issue Article 

Traumatic Brain Injury in the Pediatric Intensive Care Unit

Elora Hussain, MD

Abstract

Head trauma is a leading cause of brain injury in children, and it can have profound lifelong physical, cognitive, and behavioral consequences. Optimal acute care of children with traumatic brain injury (TBI) requires rapid stabilization and early neurosurgical evaluation by a multidisciplinary team. Meticulous attention is required to limit secondary brain injury after the initial trauma. This review discusses pathophysiology, acute stabilization, and monitoring, as well as supportive and therapeutic measures to help minimize ongoing brain injury and optimize recovery in children with TBI. [Pediatr Ann. 2018;47(7):e274–e279.]

Abstract

Head trauma is a leading cause of brain injury in children, and it can have profound lifelong physical, cognitive, and behavioral consequences. Optimal acute care of children with traumatic brain injury (TBI) requires rapid stabilization and early neurosurgical evaluation by a multidisciplinary team. Meticulous attention is required to limit secondary brain injury after the initial trauma. This review discusses pathophysiology, acute stabilization, and monitoring, as well as supportive and therapeutic measures to help minimize ongoing brain injury and optimize recovery in children with TBI. [Pediatr Ann. 2018;47(7):e274–e279.]

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in children. In the United States, approximately 475,000 children younger than age 14 years suffer from TBI annually.1 Financial burden can be significant, with pediatric inpatients accounting for over $1 billion in total charges for TBI-associated hospitalizations.2

Injury patterns due to TBI vary by age. In infants, inflicted or nonaccidental injury must always be considered. Falls are the primary mechanism of TBI-related emergency department visits in children (age 0 to 4 years). In school-age children, falls decrease with age, with a rise in bicycle accidents. In adolescents, there is a dramatic rise in TBI due to motor vehicle accidents, sports-related injuries, and violence.1

Mechanisms of Brain Injury

The distribution of damage after TBI may be focal or diffuse. Focal injury is produced by direct impact forces acting on the skull, resulting in compression of brain tissue at the site of impact (coup) or opposite the site of impact (contrecoup). Focal injuries may cause parenchymal contusions, intraparenchymal hemorrhage, subdural and epidural hematomas, and subarachnoid hemorrhage.

Diffuse injury is more widely distributed, involving the axons and vascular structures, and can be associated with hypoxic ischemic injury and cerebral edema. It is typically caused by rapid acceleration-deceleration movements of the head. Diffuse axonal injury is caused by widespread insult to cerebral white matter and may result in extended loss of consciousness.3

Clinical Injury Severity

TBI severity has classically been defined by using the Glasgow Coma Scale (GCS)4 or Pediatric GCS on admission.5 A GCS of 13 to 15 is considered mild TBI; 9 to 12 is considered moderate; and GCS less than 9 is considered severe. Frequent repeated assessments of the patient's neurologic examination and GCS are fundamental to understanding the severity and progression of illness, and to guide clinical management.6

Pathophysiology

Cerebral pathology from TBI occurs by two mechanisms: primary (or immediate) brain injury and secondary (or delayed) brain injury. Primary injury is the immediate parenchymal injury that occurs from the trauma itself. Prevention is the only measure that can affect primary injury.

In the minutes to days after primary injury, the brain is particularly vulnerable to secondary injury due to increased metabolic demands and compromised cerebral perfusion. A complex cascade of cellular, biochemical, and metabolic processes is initiated, which can lead to ongoing neuronal damage and cell death. Both cytotoxic and vasogenic edema may occur, with cytotoxic edema from cellular swelling, and vasogenic edema from disruption of the blood-brain barrier and vascular integrity.7 This phase of injury can be further exacerbated by physiologic derangements including hypoxia, hypotension, and hyperthermia.8,9 Management strategies in the acute period after TBI are primarily focused on minimizing and preventing secondary brain injury.

Evaluation

Details of the patient's medical history, timing and mechanism of the trauma, and resuscitation efforts prior to presentation are essential. On physical examination, adequacy of the patient's respiratory and cardiovascular status, as well as neurologic examination, must be rapidly assessed. Cervical spine stabilization should be maintained to avoid cervical spine injury. GCS should be determined, and life-threatening signs of impending herniation rapidly identified. These may include altered level of consciousness, pupillary dysfunction, lateralizing extremity weakness, or Cushing's triad (systemic hypertension, bradycardia, irregular respirations). The presence of Cushing's triad is a late and ominous sign of herniation.7

Initial Stabilization

If a child has normal mentation, respiratory effort, and favorable hemodynamics, advanced airway management may not be required. However, in patients with signs of airway obstruction, inadequate oxygenation or ventilation, or shock, rapid stabilization and resuscitation by a multidisciplinary team is required.

In patients with decreasing level of consciousness (and/or GCS ≤8), advanced airway support with endotracheal intubation is indicated while maintaining stabilization of the cervical spine. Strict avoidance of hypotension, hypoxemia, and intracranial hypertension are necessary during intubation.

Fluid resuscitation with isotonic solutions to reverse hypovolemic shock may be necessary and to replenish intravascular volume. Hypotonic fluid is contraindicated in the initial resuscitation as this may exacerbate cerebral edema and cell death.7

After initial stabilization, patients with moderate or severe TBI warrant emergent neuroimaging with computed tomography without contrast to assess for lesions requiring emergent neurosurgical intervention. A full trauma assessment by a multidisciplinary trauma team is also necessary to evaluate for and treat extracranial insults.

Invasive Neuromonitoring

An intracranial pressure (ICP) monitor is often placed by a neurosurgeon after stabilization in children with severe injury (GCS ≤8) for ICP monitoring and potential treatment of intracranial hypertension. This can allow for early detection of patients at risk for cerebral herniation and may allow for therapeutic drainage of cerebrospinal fluid (CSF) if needed. Current recommendations in pediatrics are for treatment of intracranial pressure ≥20 mm Hg.10

Invasive ICP monitoring is the current standard of care for children with concern for intracranial hypertension. However robust evidence supporting this practice is lacking, with only class III evidence available.10 The BEST TRIP trial published in 2012 is the only large-scale, high-quality randomized multicenter controlled trial on this subject to date, and created significant controversy regarding ICP monitoring in severe TBI.11 This trial randomized pediatric and adult patients in South America to receive either invasive ICP monitoring or treatment based on imaging and clinical examination alone.11 There was no significant difference between groups in morbidity or mortality measured at 6 months postinjury. The degree to which these results can be generalized to clinical practice in North America is controversial, due to potential differences in prehospital care and resuscitation. Although the BEST TRIP trial may not warrant a change in the current clinical practice of invasive ICP monitoring, it does highlight the need for additional investigation regarding the role of ICP monitoring in the management of severe TBI.12

Invasive and noninvasive tissue oximeters may be used in combination with ICP monitors, with studies suggesting that reduced brain tissue oxygen tension is associated with poor outcomes in severe pediatric TBI.13 Oxygenation parameters and management targets, however, are largely extrapolated from adult data.

Ongoing Management

After initial stabilization and resuscitation, ongoing physiologic monitoring and management should continue in a pediatric intensive care unit (ICU) to avoid secondary insults such as hypoxia, hypotension, and hyperthermia. In 2012, the revised Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents were published by the Brain Trauma Foundation.10 These guidelines focus on minimizing secondary brain injury after pediatric TBI and are based on best-available current evidence. Figure 1 shows an example of a clinical management pathway for severe pediatric TBI. It should be noted, however, that high quality evidence in this field remains lacking; these consensus guidelines include no level I recommendations, and most recommendations are level III evidence.9

Clinical pathway for the management of severe pediatric traumatic brain injury. CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; CT, computed tomography; EEG, electroencephalogram; EVD, external ventricular drain; ICP, intracranial pressure; IV, intravenous; GCS, Glasgow Coma Scale; MAP, mean arterial pressure; TBI, traumatic brain injury.

Figure 1.

Clinical pathway for the management of severe pediatric traumatic brain injury. CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; CT, computed tomography; EEG, electroencephalogram; EVD, external ventricular drain; ICP, intracranial pressure; IV, intravenous; GCS, Glasgow Coma Scale; MAP, mean arterial pressure; TBI, traumatic brain injury.

Intracranial Pressure and Cerebral Autoregulation

One of the most severe consequences of TBI is intracranial hypertension reflected by an elevated ICP. With a space-occupying lesion, such as an expanding hematoma or cerebral edema, initial compensatory mechanisms can prevent elevated ICP to a limited extent. Once these mechanisms are exhausted, even small increases in intra cranial volume can lead to intracranial hypertension, which can compromise cerebral perfusion and lead to cerebral ischemia, and even herniation.8

Under normal conditions, cerebral autoregulation allows the cerebral arterioles to vasodilate and vasoconstrict to maintain constant cerebral blood flow (CBF) over a wide range of blood pressures. In the clinical setting, cerebral perfusion pressure (CPP) is used as a surrogate for CBF.14 CPP is the difference between mean arterial pressure (MAP) and ICP (CPP = MAP − ICP). In healthy adults, MAP between 50 and 170 mm Hg produces little to no change in CBF. In healthy infants and children, there are few studies on the physiologic range of cerebral autoregulation.

In moderate and severe TBI, the normal mechanisms for cerebral autoregulation are often compromised, causing CBF to become dependent on MAP. Decreased CPP and cerebral ischemia may occur due to either decreased MAP or increased ICP. Conversely, increased MAP and decreased ICP may result in cerebral hyperemia.7–9 Impaired cerebral autoregulation in children is associated with worse outcomes.15 Thus, many therapeutic interventions after TBI are targeted at lowering ICP, augmenting MAP to ensure adequate CPP, and maintaining euvolemia. Pediatric guidelines recommend a minimum CPP threshold of 40 to 50 mm Hg to prevent cerebral hypoperfusion and ischemia. However, the optimal CPP in pediatric TBI is unknown.10,14

Intracranial Pressure Lowering Therapies

Patient Positioning

Maintaining the head in a neutral, midline position and elevating the head of the bed to 30 degrees has been shown in adults to reduce ICP without compromising CPP and cerebral oxygenation.16 Data in pediatrics are lacking; however, the same management is applied to children. Internal jugular catheterization is often avoided in these patients to maintain venous patency and optimize cerebral venous drainage. Care should be taken to ensure that cervical collars do not impede venous drainage.

Sedation, Analgesia, and Neuromuscular Blockade

Moderate to deep sedation is often necessary to ensure comfort and patient compliance with mechanical ventilation and treatment goals after TBI. Pain, agitation, and anxiety can also increase ICP and cerebral metabolic demand. Pediatric data on the ideal medication regimen for sedation and analgesia are lacking; however, continuous infusions of narcotics and benzodiazepines are often used in the pediatric ICU. These medications may cause further respiratory depression and hypotension, so the lowest possible doses needed for comfort and ICP management should be used. Pre-medication with lidocaine may be used prior to potentially noxious therapies such as suctioning of the endotracheal tube; however, whether lidocaine use effects clinical outcomes is unclear.17

The use of ketamine has been debated in the setting of TBI due to early studies demonstrating an association with increased ICP. More recent studies suggest that when administered in conjunction with other anesthetic agents, ICP does not increase and may even improve.18 Further studies of ketamine are needed to determine safety in the setting of pediatric TBI. Propofol is often used in adult TBI for continuous sedation; however, it is not recommended in children due to reports of metabolic acidosis, organ failure, and death, leading to safety warnings from the US Food and Drug Administration.19 Single-dose administration of etomidate may be considered for control of severe intracranial hypertension; however, the risk of adrenal suppression must be considered. Barbiturates may also be used for control of intracranial hypertension but may cause myocardial depression and systemic hypotension.10

Neuromuscular blockade is sometimes used to prevent cough, shivering, and patient-ventilator dysynchrony. Paralytics reduce metabolic demand and may result in improved chest-wall compliance, causing reduction in intrathoracic pressure to promote improved cerebral venous drainage. However, routine use of neuromuscular blockade does not improve overall outcome and is associated with prolonged ICU stay and nosocomial pneumonia and should therefore only be reserved for limited clinical situations.20

Cerebrospinal Fluid Drainage

If an external ventricular drain is placed, CSF removal may be used as a therapeutic maneuver to decrease ICP in patients with intracranial hypertension. Placement of such catheters may be technically difficult in patients with diffuse cerebral edema and compression of the lateral ventricles.8

Hyperosmolar Therapy

Mannitol and hypertonic saline are used as hyperosmolar therapies for decreasing ICP. Insufficient evidence currently exists to support the use of one therapy over the other. Mannitol has had longstanding clinical acceptance and is commonly used in both pediatric and adult TBI cases. However, there are no controlled clinical trials of mannitol use in children. Hypertonic saline, however, is gaining more acceptance and is currently supported by class II evidence for acute treatment of intracranial hypertension in children, and class III evidence to support its use as a continuous infusion.10

Mannitol is typically given in bolus doses of 0.25 to 1 g/kg and works via rapid reduction of blood viscosity and osmotic diuresis, thereby improving CBF and decreasing cerebral blood volume. Risks of mannitol administration include hypotension and renal failure, particularly when serum osmolality is >320 mOsm/L. Hypertonic saline is typically limited to 3% saline in children, but higher concentrations are often used in adults. Optimal dosing is not well studied, but bolus dosing ranges between 6.5 and 10 mL/kg, with a higher serum osmolar threshold of 360 mOsm/L. The mechanisms of hypertonic saline also include improved CBF and providing an osmotic gradient to reduce ICP. It is also thought to have theoretical benefits of inhibiting inflammation, restoring normal resting cellular membrane potential, and enhancing cardiac output.10 Potential risks include rebound in ICP, central pontine myelinolysis, and renal impairment.21

Hyperventilation

Carbon dioxide (CO2) has a profound and reversible effect on CBF, such that hypercapnia causes dilation of cerebral arteries and arterioles and increased CBF, whereas hypocapnia causes vasoconstriction and decreased CBF. Thus, hyperventilation can rapidly reduce ICP. It may be used as a brief temporizing measure for acute impending herniation, pending definitive therapy. However prophylactic, chronic hyperventilation in children should be avoided due to risks of hypoperfusion and cerebral ischemia, and normocarbia with pCO2 of 35 to 40 mm Hg should be targeted.10,22

Temperature Control

Fever in the setting of neurologic illness is associated with worse outcomes.23 Animal models and early adult studies have demonstrated benefit from therapeutic hypothermia, making it a potential neuroprotective therapy in pediatric TBI.9 However, pediatric clinical trials have not demonstrated benefit, with one trial showing a trend toward worse outcomes.24,25 Therefore, prophylactic therapeutic hypothermia is not currently recommended for management of intracranial hypertension. It may be reserved only as a temporizing measure for patients with refractory intracranial hypertension unresponsive to other medical interventions.8

Seizure Control

Post-traumatic seizures have been shown to cause persistent cerebral metabolic crisis and increased ICP.26 In children younger than age 2 years, abusive head trauma, and presence of subdural hemorrhage have been associated with increased risk of post-traumatic seizures.27 Seizures can be convulsive or nonconvulsive, with nonconvulsive seizures only detected by electroencephalogram monitoring. There is a paucity of data to guide clinicians on treatment of post-traumatic seizures; the current pediatric guidelines suggest that routine seizure prophylaxis for the first 7 days after severe TBI is reasonable to reduce the incidence of early post-traumatic seizures.10

Decompressive Craniectomy

Surgical decompressive craniectomy with duraplasty, leaving the bone flap out, may be considered for pediatric patients who have refractory intracranial hypertension unresponsive to other therapies.10 One randomized adult study, the DECRA trial, showed that decompressive craniectomy decreased ICP and ICU length of stay, but was associated with more unfavorable outcomes.28 Another recent adult study, the RESCUEicp (Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intracranial Pressure) trial, resulted in lower mortality but higher rates of severe disability and vegetative state.29 Small studies in pediatrics have shown there may be benefit in survival and neurologic outcomes,30,31 but both adult and pediatric trials have thus far been heterogeneous in both trial design and results, making it difficult to draw definitive conclusions regarding benefit from this procedure.9

Outcomes

Long-term outcomes of children with TBI are quite heterogeneous, ranging from near return to baseline to varying degrees of disability or death. Many children continue to have significant neurologic impairment at the time of discharge.9 In addition to physical disabilities, neuropsychological sequelae from TBI may influence vital development in children, such as learning, emotional awareness, and social functioning.2 Ongoing management, rehabilitation, and anticipatory guidance for a potentially new seizure disorder, or newly acquired physical, behavioral, and/or cognitive disability are important for follow-up care.

Conclusions

Care of children with TBI should focus on rapid stabilization and early neurosurgical evaluation, with ongoing management focused on prevention of secondary cerebral insults. Careful physiologic monitoring, with optimization of CPP and treatment of intracranial hypertension are critical. The paucity of high-quality literature in pediatric TBI highlights the need for further research to advance our understanding of pathophysiology and to aid in the neurologic recovery of children with TBI.

References

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Authors

Elora Hussain, MD, is the Medical Director of Neurocritical Care, Division of Pediatric Critical Care Medicine, Helen DeVos Children's Hospital; and an Assistant Professor, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine.

Address correspondence to Elora Hussain, MD, Helen DeVos Children's Hospital, 100 Michigan Street NE, MC 117, Grand Rapids, MI 49503; email: elora.hussain@helendevoschildrens.org.

Disclosure: The author has no relevant financial relationships to disclose.

10.3928/19382359-20180619-01

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